Antibiotic resistance is a well-documented phenomenon which describes the tendency of various pathogens to develop resistances to antibiotics.

Let us consider one particularly infamous instance, MRSA (methicillin-resistant staphaloccocus aureus, also known as golden staph).

What is interesting about MRSA is how rapidly it changes. Within 4-years of the mass-production of penicillin - arguably one of the most historic moments in medical science - MRSA developed immunity against it. Consequently, other antibiotics were used to treat it such as methicillin; while this was an effective remedy for a time, it's effectiveness progressively declined as new methicillin resistant strains of MRSA emerged (hence the naming of the bacterium).

But the semi-synthetic family beta-lactones were soon replaced by fully synthetic antibiotics such as quinolones and oxazolidinones. Within 13 years of the introduction linezolid (an oxazolidinone) MRSA developed a resistance to it. The same occurred with quinolones.

The point i'm trying to make here is that it is a regular occurrence for bacteria to adapt and evolve. While the desperate argument could be made that it was 'just one part of the genetic code being switched on and off' for the beta-lactones, the same cannot be said for synthetic antibiotics which never existed until 30 years ago or so. For example, linezolid operates by interrupting protein synthesis in bacteria by binding to the initiation complex, which corrupts the protein folding, hence irreparably damaging the active site. A mutation in MRSA changed the shape of the protein such that the linezolid either preferentially bound to a different part of the protein, or didn't bind at all. More about this particular mutation can be found here http://jac.oxfordjou...t/51/1/186.full

... For example, linezolid operates by interrupting protein synthesis in bacteria by binding to the initiation complex, which corrupts the protein folding, hence irreparably damaging the active site. A mutation in MRSA changed the shape of the protein such that the linezolid either preferentially bound to a different part of the protein, or didn't bind at all. More about this particular mutation can be found here...

How would you know that it is indeed a mutation and not just a variant existing in the initial population that just happens to have a differently shaped protein?

If the variant had always existed, linezolid would never have been an effective treatment for MRSA. However, in the 1990's oxazolidinones such as linezolid were the most readily administered antibiotic for MRSA precisely because it was an effective treatment.

How different is this to some rabbits being immune to mixo and then breeding. Ditto for calicivirus.

By the way, I am just asking, not making a statement.

If I have to go to hell for every rabbit, pig and roo I have shot I will be in hell for a long time, probably have my own room

Just a general observation from a shooter and also someone that kept reptiles at an advanced level.....the lower forms of life seem to evolve the quickest and best. The larger animals, like rabbits and mixo, seem to be limited to the peppered moth example.

I don't know about bacteria but with the larger life forms such as reptile and up it does seem limited to "kinds". Not much real variety except for snake, such as number of ribs and so on.

Along with reptiles I had a few cats and also white mice. rats and white rabbits for feed. Essentially the mice, rats, rabbits and cats were the same. The large lizards (monitors/goannas) could eat so much more in one go, yet they did not need to do that. In fact watching a monitor and cat of the same weight eating makes you think..what is going on here. The big lizard does not need much food but can eat enough in one go to last a long time. But the cat who needs lots of food can't eat much in one go. And give the cat a white rat and it fiddles about extracting meat but the monitor just eats the whole animal. So in short we have the animal that does not need much food but can eat so much as compared to the mammal of equal weight that can't eat much in one go and in addition can only eat part of the prey.

Something is missing from the evolution explanation.

As a side note I am inclined to think animals gravitate to an environment because of "how they are made" as opposed to evolving to be best suited for an environment.

But there does seem to be "kinds". I have always wondered why there are not big variations with mammals. Sure, there is some variation so one might do a bit better in desert conditions, kangaroo being an example. But compared to a reptile it is very poor at life in drought. Go shooting in the outback when drought is on and you will see kangaroos that are skin and bones etc. But you don't see lizards and snakes that are skin and bones. In other words why hasn't a better version of mammals evolved? Something is missing from the evolution equation.

If evolution was the complete answer then I would think there would be a whole bunch of animals between reptiles and mammals. But in either case they seem limited to "kinds" There is probably some science that explains things.

1. Some bacteria already had the resistance. For instance, when scientists at the University of Alberta revived bacteria from members of the Franklin expedition who perished in the Artic nearly 150 years ago, they found some of the bacteria were resistant to antibiotics such as clindamycin and cefoxitin Ã¢â‚¬â€œ both of which were developed more than a century after the men died. In other words, these bacteria had an inherited resistance Ã¢â‚¬â€œ the information for resistance was already in the genes. When antibiotics are used in such instances, the non-resistant bacteria die, leaving the resistant ones.

2. Some bacteria directly transfer their resistance to others. Scientists have observed an amazing process in bacteria in which a loop of DNA (information), called a plasmid, is transferred from one bacterium to another. Thus information that enables bacteria to become resistant to a substance can be transferred to a non-resistant organism. Once again, however, the information already existed Ã¢â‚¬â€œ no new information arose from matter. Information in this instance is just transferred around.

3. It is my understanding that bacteria are resistant to anti-biotics due to a deformity in the cell wall, or some other mutation that causes a loss of information, such as no longer producing an enzyme. This deformity makes them less capable of most functions compared to "normal" bacteria, and of course, it is not an addition of information.

4. In regard to the related topic of insect resistance, the famous evolutionary geneticist Francisco Ayala admitted in an article in Scientific American that in every case of insect resistance studied, the information for the resistance was already present in the genes. It was an inherited resistance Ã¢â‚¬â€œ no new information arose.

The point i'm trying to make here is that it is a regular occurrence for bacteria to adapt and evolve. While the desperate argument could be made that it was 'just one part of the genetic code being switched on and off' for the beta-lactones, the same cannot be said for synthetic antibiotics which never existed until 30 years ago.

These adaptations arise from substituting a single amino acid in a protein (normally) and long lasting resistance usually requires two substitutions. No genetic switch is involved, just a single point mutation to a single protein. If that's a valid definition of evolution, then God help us.

How would you know that it is indeed a mutation and not just a variant existing in the initial population that just happens to have a differently shaped protein?

1. Some bacteria already had the resistance. For instance, when scientists at the University of Alberta revived bacteria from members of the Franklin expedition who perished in the Artic nearly 150 years ago, they found some of the bacteria were resistant to antibiotics such as clindamycin and cefoxitin Ã¢â‚¬â€œ both of which were developed more than a century after the men died. In other words, these bacteria had an inherited resistance Ã¢â‚¬â€œ the information for resistance was already in the genes. When antibiotics are used in such instances, the non-resistant bacteria die, leaving the resistant ones.

Greater resistance to bacteria is not a new expression in the DNA. It is/was merely a previously unseen characteristic of something latent within the genome all along.

The emergence of antibiotic resistance has been observed in bacteria colonies cloned from a single non-resistant bacterium: http://www.scientifi...ial.Mutants.pdfIf the original single bacterium was non-resistant then there cannot have been anything on its genome affording resistance. The subsequently observed emergence of antibiotic resistance must therefore be a product of mutation. This then is an example of a beneficial trait emerging due to a mutation and then proliferating within the population as a result of natural selection.

Antibiotic resistance is a well-documented phenomenon which describes the tendency of various pathogens to develop resistances to antibiotics.

Let us consider one particularly infamous instance, MRSA (methicillin-resistant staphaloccocus aureus, also known as golden staph).

What is interesting about MRSA is how rapidly it changes. Within 4-years of the mass-production of penicillin - arguably one of the most historic moments in medical science - MRSA developed immunity against it. Consequently, other antibiotics were used to treat it such as methicillin; while this was an effective remedy for a time, it's effectiveness progressively declined as new methicillin resistant strains of MRSA emerged (hence the naming of the bacterium).

But the semi-synthetic family beta-lactones were soon replaced by fully synthetic antibiotics such as quinolones and oxazolidinones. Within 13 years of the introduction linezolid (an oxazolidinone) MRSA developed a resistance to it. The same occurred with quinolones.The point i'm trying to make here is that it is a regular occurrence for bacteria to adapt and evolve. While the desperate argument could be made that it was 'just one part of the genetic code being switched on and off' for the beta-lactones, the same cannot be said for synthetic antibiotics which never existed until 30 years ago or so. For example, linezolid operates by interrupting protein synthesis in bacteria by binding to the initiation complex, which corrupts the protein folding, hence irreparably damaging the active site. A mutation in MRSA changed the shape of the protein such that the linezolid either preferentially bound to a different part of the protein, or didn't bind at all. More about this particular mutation can be found here http://jac.oxfordjou...t/51/1/186.full

Thoughts?

Adsummun,Here are my thoughts? A question: How long has it been since we mapped the genome--15 years? We've done alot, but any honest molecular biologist will tell you there's much we don't know.

Another question: Since bacteria live in a molecular world--a chemical world--if they are designed, wouldn't it make sense if they could adapt to different chemicals. It only takes one mutation which can respond to a particular chemical, antibiotic, etc. and you shortly have a population.

It is no different with grasshoppers and DDT. They multiply quickly, and those that survived DDT lived and reproduced. The fact is though, is that they are still grasshoppers. The same with bacteria. They are finding new species of bacteria throughout the oceans everyday, but they are all variations of bacteria.

Finally, you forgot about the cost of change. Plieotropy is real. Revertants are real. Non- fixed traits in changing environments and conditions empirically fights against the very principles of the TOE.

If the original single bacterium was non-resistant then there cannot have been anything on its genome affording resistance. The subsequently observed emergence of antibiotic resistance must therefore be a product of mutation. This then is an example of a beneficial trait emerging due to a mutation and then proliferating within the population as a result of natural selection.

Mitch,

Most antibiotics inhibit protein synthesis. In a lot of cases, it only requires a single amino acid substitution to stop the antibody from attaching. The genes involved produce codons "Three amino acids." These codons form a chain that forms a protein. If a nonsense codon is read "Because of an antibody", then the specific gene can substitute an amino acid that the antibody isn't able to bond with. Although, it may appear beneficial at first glance, it may effect the overall fitness of the bacteria. Behe likened it to blowing up a bridge to prevent an enemy from crossing. It may have saved their lives, but they lost a bridge in the process.

If the variant had always existed, linezolid would never have been an effective treatment for MRSA. However, in the 1990's oxazolidinones such as linezolid were the most readily administered antibiotic for MRSA precisely because it was an effective treatment.

Or that variant was just a very small minority within the population that killing of the others would get MRSA manageable for the human body.

One can only be sure that it's an actual mutation by homogenizing the population. A specific strand needs to be separated and multiplied and tests would have to be done on that one. I'm not excluding your proposal, but I think that it's a valid possibility that this variant already existed, before the problems with resistance arose.

The emergence of antibiotic resistance has been observed in bacteria colonies cloned from a single non-resistant bacterium: http://www.scientifi...ial.Mutants.pdfIf the original single bacterium was non-resistant then there cannot have been anything on its genome affording resistance. The subsequently observed emergence of antibiotic resistance must therefore be a product of mutation. This then is an example of a beneficial trait emerging due to a mutation and then proliferating within the population as a result of natural selection.

Has bacteria ever become anything but bacteria?

You see the claim of evolving to the point evolutionists would have us believe always falls way short. Micro but no macro.

You see the claim of evolving to the point evolutionists would have us believe always falls way short. Micro but no macro.

He's using circular reasoning.

First, he assumes that materialistic evolution is true. Then he assumes that the bacteria didn't already have the information when it formed. Then he assumes that an increase in information at some point lead to this beneficial mutation. Then he says that this proves that materialistic evolution is true. Then the rest of the process continues and keeps repeating.

Creationists don't debate that mutations can be beneficial, our problem is when people falsely proclaim that they observed an increase of information or novel information on a genome. As to why he is trying to argue with us about beneficial mutations is anyone's guess.

(1) whether emergent resistances in MRSA are a consequence of a mutation or the proliferation of an already existent variation on the MRSA bacterium which already possessed such a resistance

(2) If it is a mutation, whether or not said mutation can be said to be beneficial

I will address (1) first. Let us assume that an antibiotic-resistant strain of MRSA was 'hiding' inside a larger non-resistant MRSA strain - and always had been. It is safe to assume then that the ratio between resistant and non-resistant MRSA will be present in equal proportions in any given sample of MRSA.

Consider three MRSA populations; one in the US, one in the UK and one in Aus. As the resistant strain is present in all of these, it should proliferate identically, and the emergent resistant MRSA strain ought to be genetically identical in each instance: that is the antibiotic resistant strain present in the US, UK and Aus are the same.

However, this is not observed. What is observed is different strains of MRSA which are all resistant to a given family of antibiotics, but are all have minor genetic nuances (i.e. usually the structure of the mecA protein) - for instance, we have EMRSA15 in the UK, ST8-USA300 in the US, and ST75-MRSA-IV in Australia. These are only single examples. There are actually hundreds of identified strains, and more are being found on a regular basis. If the original sample of MRSA consisted of hundreds of antibiotic resistant strains and hundreds of non-resistant strains, then once again, the antibiotic would never have been an effective treatment to begin with. The suggestion that they were simply 'taken care' of by the body seems wholly inadequate.

(2)

Behe likened it to blowing up a bridge to prevent an enemy from crossing. It may have saved their lives, but they lost a bridge in the process.

To assess whether or not it was a beneficial mutation, you need only ask the question of which is still alive; the mutated strain or the original strain? If the original strain is dead and the mutated strain is alive, then yes it is a beneficial mutation, whether or not that bridge is missing or not.

I am far from an expert, but we have a genetic code, and an epigenome... I am assuming bacteria have the same. The epigenome activating a genetic code that was not previously used is not evolution.

It seems to me that the two most pertinent issues here are

(1) whether emergent resistances in MRSA are a consequence of a mutation or the proliferation of an already existent variation on the MRSA bacterium which already possessed such a resistance

(2) If it is a mutation, whether or not said mutation can be said to be beneficial

I will address (1) first. Let us assume that an antibiotic-resistant strain of MRSA was 'hiding' inside a larger non-resistant MRSA strain - and always had been. It is safe to assume then that the ratio between resistant and non-resistant MRSA will be present in equal proportions in any given sample of MRSA.

Consider three MRSA populations; one in the US, one in the UK and one in Aus. As the resistant strain is present in all of these, it should proliferate identically, and the emergent resistant MRSA strain ought to be genetically identical in each instance: that is the antibiotic resistant strain present in the US, UK and Aus are the same.

However, this is not observed. What is observed is different strains of MRSA which are all resistant to a given family of antibiotics, but are all have minor genetic nuances (i.e. usually the structure of the mecA protein) - for instance, we have EMRSA15 in the UK, ST8-USA300 in the US, and ST75-MRSA-IV in Australia. These are only single examples. There are actually hundreds of identified strains, and more are being found on a regular basis. If the original sample of MRSA consisted of hundreds of antibiotic resistant strains and hundreds of non-resistant strains, then once again, the antibiotic would never have been an effective treatment to begin with. The suggestion that they were simply 'taken care' of by the body seems wholly inadequate.

(2)

Behe likened it to blowing up a bridge to prevent an enemy from crossing. It may have saved their lives, but they lost a bridge in the process.

To assess whether or not it was a beneficial mutation, you need only ask the question of which is still alive; the mutated strain or the original strain? If the original strain is dead and the mutated strain is alive, then yes it is a beneficial mutation, whether or not that bridge is missing or not.

If the variant had always existed, linezolid would never have been an effective treatment for MRSA. However, in the 1990's oxazolidinones such as linezolid were the most readily administered antibiotic for MRSA precisely because it was an effective treatment.

Or that variant was just a very small minority within the population that killing of the others would get MRSA manageable for the human body.

One can only be sure that it's an actual mutation by homogenizing the population. A specific strand needs to be separated and multiplied and tests would have to be done on that one. I'm not excluding your proposal, but I think that it's a valid possibility that this variant already existed, before the problems with resistance arose.

This is a good possibility. Variants don't have to mutate either. When they mapped our genome, they had predicted many more genes. They have found that one gene can produce variants itself. This is done by different promotors, and varying regulatory enzymes that act on the gene.

The gene might have been shut off within a small percentage of the population.

Also if there are DNA repair factors, RNA template splicers, and things as intricate as that--why could there not be regulatory splicers which cause directed mutation in response to "new" pathogens?

To assess whether or not it was a beneficial mutation, you need only ask the question of which is still alive; the mutated strain or the original strain? If the original strain is dead and the mutated strain is alive, then yes it is a beneficial mutation, whether or not that bridge is missing or not.

Also if there are DNA repair factors, RNA template splicers, and things as intricate as that--why could there not be regulatory splicers which cause directed mutation in response to "new" pathogens?

First of all, adaptations are the genes ability to produce a different amino acid codon. As AFJ pointed out; Maybe it's directed and maybe it's random. Then we have mutations, which change or alter genes or gene groups.

The fact that genes are known to produce numerous amino acid sequences, is a likely indicator that these adaptations may not be random at all. Especially, since it only took one amino acid change. The odds that many bacteria just happen to randomly mutate once in the exact spot necessary to adapt is astronomical to say the least.

According to evolutionists, mutations are random. That is why you will see organisms with different traits whether they are in the same country or a different one. The difference between the bacteria is due to interchanging, deleting, or interchanging genes, not an increase of information. This is what this discussion is about. In the end, it is still bacteria and a completely Biblical observation so the fact that bacteria can sometimes have a beneficial mutation doesn't bother me.

The question is, how can you demonstrate that the Bacteria in question's mutation is an increase(or novel) of information?

I assumed that mutations could arise and that natural selection happens; don't think anyone would argue with that.

Then he assumes that the bacteria didn't already have the information when it formed.

In the Lederberg study to which I was referring the colony was bred from a single, non-resistant individual that therefore did not have the information (for resistance) on its genome as it was non-resitant.

Then he assumes that an increase in information at some point lead to this beneficial mutation.

The colony was bred from a single, non-resistant bacterium. How else could the resistance have emerged except through a mutation?

Then he says that this proves that materialistic evolution is true. Then the rest of the process continues and keeps repeating.

No, I say: "this then is an example of a beneficial trait emerging due to a mutation and then proliferating within the population as a result of natural selection".

Creationists don't debate that mutations can be beneficial, our problem is when people falsely proclaim that they observed an increase of information or novel information on a genome. As to why he is trying to argue with us about beneficial mutations is anyone's guess.

Well, a beneficial trait that must have arisen through a mutation and then proliferates as it is naturally selected is worth pointing out.

We observe gene duplication and we observe mutations. I ask again: how can a gene that has duplicated into two, one copy of which has mutated, not amount to an increase in information on the genome? (There is no loss because of the mutation as one non-mutated copy remains.)